Regulatory volume increase in Ehrlich ascites tumor cells.
Ehrlich ascites tumor cells, shrunken as a result of KCl-depletion and Na+ loading, re-establish normal ionic concentrations by the combined activity of the Na+/K+ pump and the (2Cl- + K+ + Na+) cotransport system. Restoration of cell volume, however, correlates only with the increase in intracellular Cl-. This along with the finding that the equilibrium volume is linearly related to the steady state [Cl-] suggests that the extent to which cell volume increases is determined by Cl- transport. Net Cl- uptake, which is mediated almost exclusively by the cotransport system, is ultimately responsible for establishing the steady-state intracellular Cl- concentration. Transport mediated by this pathway ceases when the sum of the chemical potentials for Na+, K+ and Cl- approaches zero and corresponds with the establishment of a steady state for Cl-. These findings suggest that Cl- plays a key role in the regulation of net cotransport activity and thereby cell volume.
Levinson
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Department of Physiology, University of Texas Health Science Center, San Antonio 78284.
D000818:Animals; D001692:Biological Transport; D002034:Bumetanide / Q000494:pharmacology; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism* / Q000473:pathology; D002712:Chlorides / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D002712:Chlorides; D002034:Bumetanide; D012964:Sodium; D011188:Potassium